Spinal ischemia resulting in neurological complications occurs in patients sustaining a traumatic injury to the spinal cord or patients undergoing aortic surgery. Spinal cord injury can be classified as penetrating or blunt. In penetrating injuries, such as stab wound or gun shot wound to the spinal cord, complete severing of the spinal cord can occur, resulting in total muscular paralysis and loss of sensation below the level of injury. This condition of flaccid paralysis and suppression of all reflex activity following immediately upon transection of the spinal cord and involving all segments below the lesion is referred to as spinal shock. In most cases, reflex activity returns within 1 to 6 weeks from the onset of the spinal shock. Once transection of the spinal cord has occurred, peripheral reinnervation by the nervous system does not occur.
Spinal shock also occurs in blunt injuries, such as in motor vehicle accident, where compression of the spinal cord by impingement from fractured or dislocated vertebral bodies results in sensory and motor impairment below the level of cord involvement. Diagnosis of spinal fracture or dislocation is often made on X-rays. Spinal cord compression can be diagnosed on MRI, CT scan with myelogram, or lumbar puncture (Queckenstedt test). The mechanism of spinal ischemia is mostly caused by swelling of the cord. In these patients, hypotension may also occur as a result of loss of vascular sympathetic tone in the involved area. Urinary and/or bowel incontinence is a common complication due to impaired autonomic function.
Spinal ischemia is also a common postoperative complication following aortic surgeries, such as abdominal aortic aneurysmectomy. The incidence of spinal cord ischemia/stroke during aortic surgery is typically over 10%. During abdominal aortic aneurysm (AAA) repair, for example, the spinal arteries, which provide blood supply to the spinal cord, are often severed from the diseased aorta, and some but not all of which are later resutured to the prosthetic graft. As a result, blood flow to the spinal cord is reduced. When reduction of spinal perfusion lasts the duration of the surgery, typically more than forty-five minutes, spinal ischemia/stroke may ensue, often resulting in anterior spinal artery syndrome. The classic syndrome is characterized by paraplegia, rectal and urinary incontinence, loss of pain and temperature sensation, but with sparing of vibration and proprioceptive sense. Patients may also sustain neurologic deficits in the lower extremities after abdominal aortic surgery due to loss of posterior column modalities.
Brain damage associated with either stroke or head trauma is worsened by hyperthermia and improved with hypothermia. Current treatment for acute ischemic stroke and head injury is mainly supportive. A thrombolytic agent, e.g., tissue plasminogen activator (t-PA), can be administered to stroke patients who have no contraindication to t-PA. Current treatment for patients suffering from spinal injury is also supportive, e.g., to secure local hemostasis and to prevent infection by appropriate debridement, closure, and administration of antibiotics in penetrating spinal injury. In patients suffering from blunt injuries, surgical decompression of the spinal cord may be performed to restore neurological function. Spinal ischemia/stroke due to aortic surgery is also treated with supportive therapy, e.g., maintaining hemodynamic stability and monitoring neurological status, while waiting for the neurological deficits to recover with time. Therefore, besides surgical intervention in blunt injury, there is currently no good treatment which reduces neurologic damage to the spinal cord.
New devices and methods are thus needed in treating spinal ischemia/stroke in patients having spinal cord trauma or aortic surgery, in preventing spinal ischemia in patients anticipating a major thoracoabdominal surgery, or in cerebral ischemia, which minimizes neurological complication and improves the patients' quality of life without causing significant side effects.